G3iii: Describe the factors that affect output of the RV

CO = HR x SV

  • CO of RV depends on:
  1. HR
  2. Preload of RV
  3. Contractility of RV
  4. Afterload of RV
  5. Ventricular interdependence

1. Heart Rate

  • ↑HR = ↓diastolic filling time = ↓preL = ↓CO
  • Set by the pacemaker activity of the SA node
  • Influenced by ANS; ↑symp. stimulation = ↑HR = ↑CO (but adversely affects preload)

2. PRELOAD OF RV = the load on myocardial fibres just prior to the onset of contraction & is the sarcomere length at end diastole

  • By F – S Law, ↑preL = ↑SV = ↑CO

Venous Pressure

  • ↑venous pressure = ↑venous return = ↑preL = ↑CO
  • Venous P depends on:
    • Total Blood Volume
    • Gravity
    • Muscle contraction
    • Venous compliance

Ventricular Compliance

    • ↑compliance = ↑EDV = ↑preL = ↑CO

HR

  • ↓HR = ↑filling time = ↑EDV = ↑preL = ↑CO

Atrial Contraction

    • Atrial kick = 10 – 40% ventricular filling
    • ∴loss of atrial kick = ↓EDV = ↓preL = ↓CO

Inflow Resistance

  • ↑inflow resistance (mitral stenosis) = ↓EDV = ↓preL = ↓CO

Outflow Resistance

    • ↑outflow resistance (↑PAP) = ↑EDV = ↑preL = ↑CO

Ventricular Inotropy

  • Ventricle systolic failure = ↓emptying = ↑preL = ↑CO (to a point)

3. Contractility = the intrinsic ability of cardiac fibres to shorten, independent of preL/afterL

  • ↑contractility = ↑CO
  • Contractility dependent on:
    • Substrate availability
    • Coronary blood supply
    • Myofilament integrity
    • Intracellular [Ca2+] availability
    • Metabolic homeostasis: O2, pH, K+, temp

4. Afterload

  • Afterload = sum of all factors required to overcome so that blood may be ejected from ventricle to circulation
  • AfterL gives rise to wall tension
  • ∴afterL can be thought of as the wall tension required to overcome impedance to eject blood
  • Factors affecting afterL =
    1. Wall tension factors
    2. Outflow factors 
  • Wall tension
Wall Tension
    • TRANSMURAL P = intraventricular P – intrapleural P
    • ∴↓intrapleural P = ↑transmural P = ↑afterL = ↓CO
    • Thickness → RV thin walled & used to operating against low R
    • Radius → ↑radius (i.e. saddle PE) = ↑wall T= ↑afterL = ↓CO 
  • Outflow
    • Because the RV is unique & operates a low P system, the resistance in pulm. vessels is the main determinant of afterL & ∴CO
    • Pulmonary vascular resistance
R
    • CO, O2, pH, resp cycle all affect vessel radius
    • ↓radius = ↑R = ↑afterL = ↓CO
  • Outflow tract resistance
    • ↑outflow tract R (i.e. PE) = ↑afterL = ↓CO
  • Root pressure/compliance
    • ↑PAP/↓pulm root compliance = ↑afterL = ↓CO
    • Any cause of pulmonary HTN (CVF, MR/MS, chronic lung disease, multiple PE) will ↑PAP
    • Pulmonary stenosis = ↓compliance

5. Ventricular Interdependence

  • 20 – 40% RV contraction provided from LV via IV septum ∴LV failure → RV dysfunction
  • Conversely ↑RV afterL → RV dilatation → deviation of IV septum into LV → ↓LV preL → ↓LV CO → ↓VR to RV → ↓RV CO